|Computed Breakpoints include||[60C4-60C4];[60C7-60C7];|
|Map ( GBrowse )||
|Member of large scale dataset(s)|
A set of isogenic deficiency stocks created by FLP-induced recombination between FRT-carrying transgenic insertions; molecularly defined deletion endpoints correspond to initial location of the progenitor insertions. Initial set of 519 isogenic deletions provides 56% genome coverage.
The current Exelixis collection at the Bloomington Stock Center differs from the original described in FBrf0175003: a significant number were shown not to carry a deletion and have been removed from the collection; a number of stocks have been lost; a number of additional deletions are included that were generated after publication.
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|Nature of the Aberration|
|Class of aberration (relative to progenitor)|
|Formalized genetic data|
|Genetic mapping information|
|Comments on Cytology|
|Gene Deletion & Duplication Data|
|Genes Deleted / Disrupted|
|Genes NOT Deleted / Disrupted|
|Genes NOT Duplicated|
|In combination with other aberrations|
|NOT in combination with other aberrations|
Homozygotes show lethality at late stages of embryogenesis. The body wall muscles develop correctly in the mutant embryos and attach to the epidermis as in wild type. The gut elongates and forms gut constrictions in the mutant embryos and the visceral muscles develop normally. Cardioblasts of the dorsal vessel and macrophages are shaped normally in the mutant embryos. At the end of embryogenesis the mutant embryos are able to move in the eggshell and can contract their muscles (although not as frequently or as vigorously as wild type), but they do not hatch.
|Stocks ( 1 )|
|Notes on Origin|
|Balancer / Genotype Variants of the Aberration|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 10 )|
|Personal communication to FlyBase|